Abstract

Senescence Accelerated Mouse (SAM) shows an earlier onset and irreversible advancement of senescence manifested by the following signs and lesions: a loss of activity, skin coarseness, a shortened life span, systemic senile amyloidosis, senile cataract,senile osteoporosis1–3 etc. Further, it was reported that SAM-P/8, a substrain of accelerated senescence prone series with a low incidence of senile amyloidosis, showed the following age-related deterioration in learning ability: SAM-P/8 as well as SAM-P/8/Ta, which is SAM-P/8 bred under specific pathogen-free conditions, exhibited remarkable age-related deterioration in memory and learning in passive avoidance response and hyperactivity in the open field, compared with SAM-R/1 control, a substrain of accelerated senescence resistant series4–5. In searching for the structural basis of such behavioral changes and accelerated senescence, we found age-related pathomorphological changes in the SAM-P/8 brain3. Several changes related to the learning and memory deficits are described herein.